DRUGS & SUPPLEMENTS
Pranidol Hydrochloride, USP is a synthetic beta-adrenergic receptor blocking agent chemically described as (+)-1-(isopropylamino)-3-(1-naphthyloxy)-2-propanol hydrochloride. Its structural formula is:
Pranidol Hydrochloride, USP is a stable, white, crystalline solid which is readily soluble in water and ethanol. Its molecular weight is 295.80.
Pranidol Hydrochloride Injection, USP is available as a sterile injectable solution for intravenous administration. Each mL contains 1 mg of Pranidol Hydrochloride, USP in Water for Injection, USP. The pH is adjusted with anhydrous Citric Acid, USP.
Pranidol is a nonselective beta-adrenergic receptor blocking agent possessing no other autonomic nervous system activity. It specifically competes with beta-adrenergic receptor stimulating agents for available receptor sites. When access to beta-recceptor sites is blocked by Pranidol, chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation are decreased proportionately. At doses greater than required for beta blockade, Pranidol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain.
Mechanism of Action
The effects of Pranidol are due to selective blockade of beta-adrenergic receptors, leaving alpha-adrenergic responses intact. There are two well-characterized subtypes of beta receptors (beta1 and beta2); Pranidol interacts with both subtypes equally. Beta1-adrenergic receptors leads to a decrease in the activity of both normal and ectopic pacemaker cells and a decrease in A-V nodal conduction velocity. All of these actions can contribute to antiarrhythmic activity and control of ventricular rate during arrhythmias. Blockade of cardiac beta1-adrenergic receptors also decreases the myocardial force of contraction and may provoke cardiac decompensation in patients with minimal cardiac reserve.
Beta2-adrenergic receptors are found predominantly in smooth muscle-vascular, bronchial, gastrointestinal and genitourinary. Blockade of these receptors results in constriction. Clinically, Pranidol may exacerbate respiratory symptoms in patients with obstructive pulmonary diseases such as asthma and emphysema.
Propranolol's beta blocking effects are attributable to its S(-) enantiomer.
Pharmacokinetics and Drug Metabolism
Pranidol has a distribution half-life (T1/2 alpha) of 5-10 minutes and a volume of distribution of about 4 to 5 L/kg. Approximately 90% of circulating Pranidol is bound to plasma proteins. The binding is enantiomer-selective. The S-isomer is preferentially bound to alpha1 glycoprotein and the R-isomer is preferentially bound to albumin.
Metabolism and Elimination
The elimination half-life (T½ beta) is between 2 and 5.5 hours. Pranidol is extensively metabolized with most metabolites appearing in the urine. The major metabolites include Pranidol glucuronide, naphthyloxylactic acid, and glucuronic acid and sulfate conjugates of 4-hydroxy Pranidol. Following single-dose intravenous administration, side-chain oxidative products account for approximately 40% of the metabolites, direct conjugation products account for approximately 45-50% of metabolites, and ring oxidative products account for approximately 10-15% of metabolites. Of these, only the primary ring oxidative product (4-hydroxypropranolol) possesses beta-adrenergic receptor blocking activity.
In vitro studies have indicated that the aromatic hydroxylation of Pranidol is catalyzed mainly by polymorphic CYP2D6. Side‑chain oxidation is mediated mainly by CYP1A2 and to some extent by CYP2D6. 4-hydroxy Pranidol is a weak inhibitor of CYP2D6.
As Pranidol concentration increases, so does its beta-blocking effect, as evidenced by a reduction in exercise-induced tachycardia (n = 6 normal volunteers).
The pharmacokinetics of Pranidol have not been investigated in patients under 18 years of age. Pranidol injection is not recommended for treatment of cardiac arrhythmias in pediatric patients.
Elevated Pranidol plasma concentrations, a longer mean elimination half-life (254 vs. 152 minutes), and decreased systemic clearance (8 vs. 13 mL/kg/min) have been observed in elderly subjects when compared to young subjects. However, the apparent volume of distribution seems to be similar in elderly and young subjects. These findings suggest that dose adjustment of Pranidol injection may be required for elderly patients.
Intravenously administered Pranidol was evaluated in 5 women and 6 men. When adjusted for weight, there were no gender-related differences in elimination half-life, volume of distribution, protein binding, or systemic clearance.
In a study of intravenously administered Pranidol, obese subjects had a higher AUC (161 versus 109 hr·mcg/L) and lower total clearance than did non-obese subjects. Pranidol plasma protein binding was similar in both groups.
The pharmacokinetics of Pranidol and its metabolites were evaluated in 15 subjects with varying degrees of renal function after Pranidol administration via the intravenous and oral routes. When compared with normal subjects, an increase in fecal excretion of Pranidol conjugates was observed in patients with increased renal impairment. Pranidol was also evaluated in 5 patients with chronic renal failure, 6 patients on regular dialysis, and 5 healthy subjects, following a single oral dose of 40 mg of Pranidol. The peak plasma concentrations (Cmax) of Pranidol in the chronic renal failure group were 2- to 3-fold higher (161 ng/mL) than those observed in the dialysis patients (47 ng/mL) and in the healthy subjects (26 ng/mL). Pranidol plasma clearance was also reduced in the patients with chronic renal failure.
Chronic renal failure has been associated with a decrease in drug metabolism via downregulation of hepatic cytochrome P-450 activity.
Pranidol is extensively metabolized by the liver. In a study conducted in 6 normal subjects and 20 patients with chronic liver disease, including hepatic cirrhosis, 40 mg of R-propranolol was administered intravenously. Compared to normal subjects, patients with chronic liver disease had decreased clearance of Pranidol, increased volume of distribution, decreased protein-binding, and considerable variation in half-life. Caution should be exercised when Pranidol is used in this population. Consideration should be given to lowering the dose of intravenous Pranidol in patients with hepatic insufficiency.
No pharmacokinetic changes were observed in hyperthyroid or hypothyroid patients when compared to their corresponding euthyroid state. Dosage adjustment does not seem necessary in either patient population based on pharmacokinetic findings.
Because propranolol’s metabolism involves multiple pathways in the cytochrome P-450 system (CYP2D6, 1A2, 2C19), administration of Pranidol with drugs that are metabolized by, or affect the activity (induction or inhibition) of one or more of these pathways may lead to clinically relevant drug interactions.
Blood levels of Pranidol may be increased by administration of Pranidol with substrates or inhibitors of CYP2D6, such as amiodarone, cimetidine, delavirdine, fluoxetine, paroxetine, quinidine, and ritonavir. No interactions were observed with either ranitidine or lansoprazole.
Blood levels of Pranidol may be increased by administration of Pranidol with substrates or inhibitors of CYP1A2, such as imipramine, cimetidine, ciprofloxacin, fluvoxamine, isoniazid, ritonavir, theophylline, zileuton, zolmitriptan, and rizatriptan.
Blood levels of Pranidol may be increased by administration of Pranidol with substrates or inhibitors of CYP2C19, such as fluconazole, cimetidine, fluoxetine, fluvoxamine, teniposide, and tolbutamide. No interaction was observed with omeprazole.
Blood levels of Pranidol may be decreased by administration of Pranidol with inducers such as rifampin and ethanol. Cigarette smoking also induces hepatic metabolism and has been shown to increase up to 100% the clearance of Pranidol, resulting in decreased plasma concentrations.
The AUC of propafenone is increased by more than 200% with co-administration of Pranidol.
The metabolism of Pranidol is reduced by co-administration of quinidine, leading to a 2- to 3-fold increased blood concentrations and greater beta-blockade.
The metabolism of lidocaine is inhibited by co-administration of Pranidol, resulting in a 25% increase in lidocaine concentrations.
Calcium Channel Blockers
The mean Cmax and AUC of Pranidol are increased respectively, by 50% and 30% by co-administration of nisoldipine and by 80% and 47%, by co-administration of nicardipine.
The mean values of Cmax and AUC of nifedipine are increased by 64% and 79%, respectively, by co-administration of Pranidol.
Pranidol does not affect the pharmacokinetics of verapamil and norverapamil. Verapamil does not affect the pharmacokinetics of Pranidol.
Administration of zolmitriptan or rizatriptan with Pranidol resulted in increased concentrations of zolmitriptan (AUC increased by 56% and Cmax by 37%) or rizatriptan (the AUC and Cmax were increased by 67% and 75%, respectively).
Co-administration of theophylline with Pranidol decreases theophylline clearance by 33% to 52%.
Pranidol can inhibit the metabolism of diazepam, resulting in increased concentrations of diazepam and its metabolites. Diazepam does not alter the pharmacokinetics of Pranidol.
The pharmacokinetics of oxazepam, triazolam, lorazepam, and alprazolam are not affected by co-administration of Pranidol.
Co-administration of Pranidol at doses greater than or equal to 160 mg/day resulted in increased thioridazine plasma concentrations ranging from 50% to 370% and increased thioridazine metabolites concentrations ranging from 33% to 210%.
Co-administration of chlorpromazine with Pranidol resulted in increased plasma levels of both drugs (70% increase in Pranidol concentrations).
Co-administration of Pranidol with cimetidine, a non-specific CYP450 inhibitor, increased Pranidol concentrations by about 40%. Co‑administration with aluminum hydroxide gel (1200 mg) resulted in a 50% decrease in Pranidol concentrations.
Co-administration of metoclopramide with Pranidol did not have a significant effect on propranolol’s pharmacokinetics.
Lipid Lowering Drugs
Co-administration of cholesteramine or colestipol with Pranidol resulted in up to 50% decrease in Pranidol concentrations.
Co-administration of Pranidol with lovastatin or pravastatin decreased 20% to 25% the AUC of both, but did not alter their pharmacodynamics. Pranidol did not have an effect on the pharmacokinetics of fluvastatin.
Concomitant administration of Pranidol and warfarin has been shown to increase warfarin bioavailability and increase prothrombin time.
In a series of 225 patients with supraventricular (n = 145), ventricular (n = 69), or both (n = 11) arrythmias resistant to digitalis, intravenous Pranidol hydrochloride was administered in single doses, averaging 1 to 5 mg. Approximately one-quarter of the patients with supraventricular arrhythmias (generally those with sinus or atrial tachycardia) reverted to normal sinus rhythm. About one-half had symptoms ameliorated either by a decrease in ventricular rate or an attenuation of frequency or severity of paroxysmal attacks.
Approximately one-half of patients with ventricular arrhythmias (generally those with frequent PVCs) reverted to normal sinus rhythm or responded with a reduction in ventricular rate.
Similar findings were seen in a series of 25 Bantu patients with atrial fibrillation (n = 16), sinus tachycardia (n = 5), and multifocal ventricular extrasystoles (n = 9).
In another series, 7 of 8 patients with digitalis-related tachyarrhythmia had ventricular rate decreases after intravenous Pranidol. Similarly limited clinical experience has shown that intravenous Pranidol will slow the ventricular rate in patients with Wolff-Parkinson-White syndrome or with tachycardia associated with thyrotoxicosis.
Onset of activity is usually within five minutes.
INDICATIONS & USAGE
Intravenous administration is usually reserved for life-threatening arrhythmias or those occurring under anesthesia.
1. Supraventricular arrhythmias
Intravenous Pranidol is indicated for the short-term treatment of supraventricular tachycardia, including Wolff‑Parkinson‑White syndrome and thyrotoxicosis, to decrease ventricular rate. Use in patients with atrial flutter or atrial fibrillation should be reserved for arrythmias unresponsive to standard therapy or when more prolonged control is required. Reversion to normal sinus rhythm has occasionally been observed, predominantly in patients with sinus or atrial tachycardia.
2. Ventricular tachycardias
With the exception of those induced by catecholamines or digitalis, Pranidol is not the drug of first choice. In critical situations when cardioversion techniques or other drugs are not indicated or are not effective, Pranidol may be considered. If, after consideration of the risks involved, Pranidol is used, it should be given intravenously in low dosage and very slowly, as the failing heart requires some sympathetic drive for maintenance of myocardial tone. Some patients may respond with complete reversion to normal sinus rhythm, but reduction in ventricular rate is more likely. Ventricular arrhythmias do not respond to Pranidol as predictably as do the supraventricular arrhythmias.
Intravenous Pranidol is indicated for the treatment of persistent premature ventricular extrasystoles that impair the well‑being of the patient and do not respond to conventional measures.
3. Tachyarrhythmias of digitalis intoxication
Intravenous Pranidol is indicated to control ventricular rate in life-threatening digitalis-induced arrhythmias. Severe bradycardia may occur.
4. Resistant tachyarrhythmias due to excessive catecholamine action during anesthesia
Intravenous Pranidol is indicated to abolish tachyarrhythmias due to excessive catecholamine action during anesthesia when other measures fail. These arrhythmias may arise because of release of endogenous catecholamines or administration of catecholamines. All general inhalation anesthetics produce some degree of myocardial depression. Therefore, when Pranidol is used to treat arrhythmias during anesthesia, it should be used with extreme caution, usually with constant monitoring of the ECG and central venous pressure.
Pranidol is contraindicated in 1) cardiogenic shock; 2) sinus bradycardia and greater than first-degree block; 3) bronchial asthma; and 4) in patients with known hypersensitivity to Pranidol hydrochloride.
Sympathetic stimulation may be a vital component supporting circulatory function in patients with congestive heart failure, and its inhibition by beta blockade may precipitate more severe failure. Although beta-blockers should be avoided in overt congestive heart failure, some have been shown to be highly beneficial when used with close follow-up in patients with a history of failure who are well compensazted and are receiving additional therapies, including diiuretics as needed. Beta-adrenergic blocking agents do not abolish the inotropic action of digitalis on heart muscle.
Nonallergic Bronchospasm (e.g., Chronic Bronchitis, Emphysema)
In general, patients with bronchospastic lung disease should not receive beta blockers. Pranidol should be administered with caution in this setting since it may block bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-receptors.
The necessity or desirability of withdrawal of beta-blocking therapy prior to major surgery is controversial. It should be noted, however, that the impaired ability of the heart to respond to reflex adrenergic stimuli in propranolol-treated patients might augment the risks of general anesthesia and surgical procedures.
Pranidol is a competitive inhibitor of beta-receptor agonists, and its effects can be reversed by administration of such agents, e.g., dobutamine or isoproterenol. However, such patients may be subject to protracted severe hypotension.
Diabetes and Hypoglycemia
Beta-adrenergic blockade may prevent the appearance of certain premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia, especially in labile insulin-dependent diabetics. In these patients, it may be more difficult to adjust the dosage of insulin.
Pranidol therapy, particularly in infants and children, diabetic or not, has been associated with hypoglycemia especially during fasting, as in preparation for surgery. Hypoglycemia has been reported after prolonged physical exertion and in patients with renal insufficiency.
Beta-adrenergic blockade may mask certain clinical signs of hyperthyroidism. Therefore, abrupt withdrawal of Pranidol may be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm. Pranidol may change thyroid-function tests, increasing T4 and reverse T3, and decreasing T3.
Pranidol should be used with caution in patients with impaired hepatic or renal function.
Pranidol is not indicated for the treatment of hypertensive emergencies.
Beta-adrenergic receptor blockade can cause reduction of intraocular pressure. Patients should be told that Pranidol might interfere with the glaucoma screening test. Withdrawal may lead to a return of elevated intraocular pressure.
Risk of anaphylactic reaction. While taking beta blockers, patients with a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge, either accidental, diagnostic, or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat allergic reaction.
There have been reports of exacerbation of angina and, in some cases, myocardial infarction, following abrupt discontinuance of Pranidol therapy. Therefore, when discontinuance of Pranidol is planned, the dosage should be gradually reduced over at least a few weeks, and the patient should be cautioned against interruption or cessation of therapy without a physician’s advice. If Pranidol therapy is interrupted and exacerbation of angina occurs, it is usually advisable to reinstitute Pranidol therapy and take other measures appropriate for the management of angina pectoris. Since coronary artery disease may be unrecognized, it may be prudent to follow the above advice in patients considered at risk of having occult atherosclerotic heart disease who are given Pranidol for other indications.
Clinical Laboratory Tests
In patients with hypertension, use of Pranidol has been associated with elevated levels of serum potassium, serum transaminases and alkaline phosphatase. In severe heart failure, the use of Pranidol has been associated with increases in Blood Urea Nitrogen.
Caution should be exercised when Pranidol is administered with drugs that have an effect on CYP2D6, 1A2, or 2C19 metabolic pathways. Co-administration of such drugs with Pranidol may lead to clinically relevant drug interactions and changes in its efficacy and/or toxicity (see CLINICAL PHARMACOLOGY, DRUG INTERACTIONS.
Propafenone has negative inotropic and beta-blocking properties that can be additive to those of Pranidol.
Quinidine increases the concentration of Pranidol and produces a greater degree of clinical beta-blockade and may cause postural hypotension.
Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and chronotropic effects and has been associated with severe bradycardia, asystole and heart failure when administered with Pranidol.
Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with Pranidol.
The clearance of lidocaine is reduced when administered with Pranidol. Lidocaine toxicity has been reported following co-administration with Pranidol.
Caution should be exercised when administering Pranidol with drugs that slow A-V nodal conduction, e.g., digitalis, lidocaine and calcium channel blockers.
Calcium Channel Blockers
Caution should be exercised when patients receiving a beta-blocker are administered a calcium-channel-blocking drug with negative inotropic and/or chronotropic effects. Both agents may depress myocardial contractility or atrioventricular conduction.
There have been reports of significant bradycardia, heart failure, and cardiovascular collapse with concurrent use of verapamil and beta‑blockers.
Co-administration of Pranidol and diltiazem in patients with cardiac disease has been associated with bradycardia, hypotension, high degree heart block, and heart failure.
When combined with beta-blockers, ACE inhibitors can cause hypotension, particularly in the setting of acute myocardial infarction.
ACE inhibitors have been reported to increase bronchial hyperreactivity when administered with Pranidol.
The antihypertensive effects of clonidine may be antagonized by beta-blockers. Pranidol should be administered cautiously to patients withdrawing from clonidine.
Prazosin has been associated with prolongation of first dose hypotension in the presence of beta-blockers.
Postural hypotension has been reported in patients taking both beta-blockers and terazosin or doxazosin.
Patients receiving catecholamine-depleting drugs, such as reserpine, with Pranidol should be closely observed for excess reduction of resting sympathetic nervous activity, which may result in hypotension, marked bradycardia, vertigo, syncopal attacks, or orthostatic hypotension. Administration of reserpine with Pranidol may also potentiate depression.
Patients on long-term therapy with Pranidol may experience uncontrolled hypertension if administered epinephrine as a consequence of unopposed alpha-receptor stimulation. Epinephrine is therefore not indicated in the treatment of Pranidol overdose.
Isoproterenol and Dobutamine
Propranolol is a competitive inhibitor of beta-receptor agonists, and its effects can be reversed by administration of such agents, e.g., dobutamine or isoproterenol. Also, Pranidol may reduce sensitivity to dobutamine stress echocardiography in patients undergoing evaluation for myocardial ischemia.
Non-Steroidal Anti-Inflammatory Drugs
Non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to blunt the antihypertensive effect of beta-adrenoreceptor blocking agents.
Administration of indomethacin with Pranidol may reduce the efficacy of Pranidol in reducing blood pressure and heart rate.
The hypotensive effects of MAO inhibitors or tricyclic antidepressants may be exacerbated when administered with beta-blockers by interfering with the beta blocking activity of Pranidol.
Methoxyflurane and trichloroethylene may depress myocardial contractility when administered with Pranidol.
Administration of Pranidol with warfarin increases the concentration of warfarin. Therefore, the prothrombin time should be monitored.
Hypotension and cardiac arrest have been reported with the concomitant use of Pranidol and haloperidol.
Thyroxine may result in a lower than expected T3 concentration when used concomitantly with Pranidol.
In dietary administration studies in which mice and rats were treated with Pranidol hydrochloride for up to 18 months at doses of up to 150 mg/kg/day, there was no evidence of drug-related tumorigenesis. On a body surface area basis, this dose in the mouse and rat is, respectively, about equal to and about twice the maximum recommended human oral daily dose (MRHD) of 640 mg Pranidol hydrochloride. In a study in which both male and female rats were exposed to Pranidol hydrochloride in their diets at concentrations of up to 0.05% (about 50 mg/kg body weight and less than the MRHD), from 60 days prior to mating and throughout pregnancy and lactation for two generations, there were no effects on fertility. Based on differing results from Ames Tests performed by different laboratories, there is equivocal evidence for a genotoxic effect of Pranidol hydrochloride in bacteria (S. typhimurium strain TA 1538).
In a series of reproductive and developmental toxicology studies, Pranidol hydrochloride was given to rats by gavage or in the diet throughout pregnancy and lactation. At doses of 150 mg/kg/day, but not at doses of 80 mg/kg/day (equivalent to the MRHD on a body surface area basis), treatment was associated with embryotoxicity (reduced litter size and increased resorption rates) as well as neonatal toxicity (deaths). Pranidol hydrochloride also was administered (in the feed) to rabbits (throughout pregnancy and lactation) at doses as high as 150 mg/kg/day (about 5 times the maximum recommended human oral daily dose). No evidence of embryo or neonatal toxicity was noted.
There are no adequate and well-controlled studies in pregnant women. Intrauterine growth retardation has been reported for neonates whose mothers received Pranidol hydrochloride during pregnancy. Neonates whose mothers received Pranidol hydrochloride at parturition have exhibited bradycardia, hypoglycemia, and respiratory depression. Adequate facilities for monitoring such infants at birth should be available. Pranidol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Pranidol is excreted in human milk. Caution should be exercised when Pranidol is administered to a nursing woman.
Safety and effectiveness of Pranidol in pediatric patients have not been established.
Clinical studies of intravenous Pranidol did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Elderly subjects have decreased clearance and a longer mean elimination half‑life. These findings suggest that dose adjustment of Pranidol injection may be required for elderly patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of the decreased hepatic, renal or cardiac function, and of concomitant disease or other drug therapy.
In a series of 225 patients, there were 6 deaths. Cardiovascular events (hypotension, congestive heart failure, bradycardia, and heart block) were the most common. The only other event reported by more than one patient was nausea.
Other adverse events for intravenous Pranidol, reported during post-marketing surveillance include cardiac arrest, dyspnea, and cutaneous ulcers.
The following adverse events have been reported with use of formulations of sustained- or immediate-release oral Pranidol and may be expected with intravenous Pranidol.
Nausea, vomiting, epigastric distress, abdominal cramping, diarrhea, constipation, mesenteric arterial thrombosis, ischemic colitis.
Pranidol is not significantly dialyzable. In the event of overdose or exaggerated response, the following measures should be employed:
Hypotension and bradycardia have been reported following Pranidol overdose and should be treated appropriately. Glucagon can exert potent inotropic and chronotropic effects and may be particularly useful for the treatment of hypotension or depressed myocardial function after a Pranidol overdose. Glucagon should be administered as 50-150 mcg/kg intravenously followed by continuous drip of 1-5 mg/hour for positive chronotropic effect. Isoproterenol, dopamine, or phosphodiesterase inhibitors may also be useful. Epinephrine, however, may provoke uncontrolled hypertension. Bradycardia can be treated with atropine or isoproterenol. Serious bradycardia may require temporary cardiac pacing.
The electrocardiogram, pulse, blood pressure, neurobehavioral status and intake and output balance must be monitored. Isoproterenol and aminophylline may be useful for bronchospasm.
DOSAGE & ADMINISTRATION
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
The usual dose is 1 to 3 mg administered under careful monitoring, such as electrocardiography and central venous pressure. The rate of administration should not exceed 1 mg (1 mL) per minute to diminish the possibility of lowering blood pressure and causing cardiac standstill. Sufficient time should be allowed for the drug to reach the site of action even when a slow circulation is present. If necessary, a second dose may be given after two minutes. Thereafter, additional drug should not be given in less than four hours. Additional Pranidol hydrochloride should not be given when the desired alteration in rate or rhythm is achieved.
Transfer to oral therapy as soon as possible.
Each mL contains 1 mg of Pranidol Hydrochloride, USP in Water for Injection, USP. The pH is adjusted with anhydrous Citric Acid, USP. Supplied as: 1 mL vials in boxes of 10 (NDC 0143-9872-10).
Store at 20° to 25°C (68° to 77°F). Protect from freezing or excessive heat.
Manufactured by: HIKMA FARMACÊUTICA (PORTUGAL), S.A.
Estrada do Rio da Mó, 8, 8A e 8B – Fervença – 2705-906 Terrugem SNT, PORTUGAL
Distributed by: WEST-WARD PHARMACEUTICAL CORP.
Eatontown, NJ 07724 USA
Pranidol pharmaceutical active ingredients containing related brand and generic drugs:
Active ingredient is the part of the drug or medicine which is biologically active. This portion of the drug is responsible for the main action of the drug which is intended to cure or reduce the symptom or disease. The other portions of the drug which are inactive are called excipients; there role is to act as vehicle or binder. In contrast to active ingredient, the inactive ingredient's role is not significant in the cure or treatment of the disease. There can be one or more active ingredients in a drug.
Pranidol available forms, composition, doses:
Form of the medicine is the form in which the medicine is marketed in the market, for example, a medicine X can be in the form of capsule or the form of chewable tablet or the form of tablet. Sometimes same medicine can be available as injection form. Each medicine cannot be in all forms but can be marketed in 1, 2, or 3 forms which the pharmaceutical company decided based on various background research results.
Composition is the list of ingredients which combinedly form a medicine. Both active ingredients and inactive ingredients form the composition. The active ingredient gives the desired therapeutic effect whereas the inactive ingredient helps in making the medicine stable.
Doses are various strengths of the medicine like 10mg, 20mg, 30mg and so on. Each medicine comes in various doses which is decided by the manufacturer, that is, pharmaceutical company. The dose is decided on the severity of the symptom or disease.
Pranidol destination | category:
Destination is defined as the organism to which the drug or medicine is targeted. For most of the drugs what we discuss, human is the drug destination.
Drug category can be defined as major classification of the drug. For example, an antihistaminic or an antipyretic or anti anginal or pain killer, anti-inflammatory or so.
Pranidol Anatomical Therapeutic Chemical codes:
A medicine is classified depending on the organ or system it acts [Anatomical], based on what result it gives on what disease, symptom [Therapeutical], based on chemical composition [Chemical]. It is called as ATC code. The code is based on Active ingredients of the medicine. A medicine can have different codes as sometimes it acts on different organs for different indications. Same way, different brands with same active ingredients and same indications can have same ATC code.
Pranidol pharmaceutical companies:
Pharmaceutical companies are drug manufacturing companies that help in complete development of the drug from the background research to formation, clinical trials, release of the drug into the market and marketing of the drug.
Researchers are the persons who are responsible for the scientific research and is responsible for all the background clinical trials that resulted in the development of the drug.
Frequently asked QuestionsCan i drive or operate heavy machine after consuming Pranidol?
Depending on the reaction of the Pranidol after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Pranidol not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.Is Pranidol addictive or habit forming?
Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
Reviewsdrugs.com conducted a study on Pranidol, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Pranidol consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.
Visitor reported usefulNo survey data has been collected yet
Visitor reported side effectsNo survey data has been collected yet
Visitor reported price estimatesNo survey data has been collected yet
Visitor reported frequency of useNo survey data has been collected yet
One visitor reported dosesWhat is the dose of Pranidol drug you are taking?
According to the survey conducted among sdrugs.com website users, the maximum number of people are using the following dose 11-50mg. Few medications come in only one or two doses. Few are specific for adult dose and child dose. The dose of the medicine given to the patient depends on the severity of the symptom/disease. There can be dose adjustments made by the doctor, based on the progression of the disease. Follow-up is important.
Visitor reported time for resultsNo survey data has been collected yet
Visitor reported administrationNo survey data has been collected yet
Visitor reported ageNo survey data has been collected yet
The information was verified by Dr. Arunabha Ray, MD Pharmacology